From the Programmed Aging Camp
Here is an open access paper from a researcher who focuses on mTOR and sees aging as almost entirely programmed, not the consequence of stochastic damage. His view as outlined in the paper is analogous to the view of nuclear DNA damage as not being significant over the present human life span. I think he has a very large hill of evidence for the damage-based view of aging to overcome in order to make a convincing point, however, and this should serve as a reminder that there are a great many diverse (but not necessarily well supported) views in the scientific community when it comes to the nuts and bolts of aging: "Aging is defined as a decline caused by accumulation of all sorts of damage, in particular, molecular damage. This statement seemed so obvious that it was not questioned. Yet several lines of evidence rule out molecular damage as a cause of aging. Yes, of course, molecular damage accumulates over time. But this accumulation is not sufficient to cause organismal death. Eventually it would. But the organism does not live long enough, because another cause terminates life first. This cause is aging, a continuation of developmental growth. Definitely, developmental growth is not driven by accumulation of molecular damage, although molecular damage accumulates. Similarly, aging is not driven by damage. Growth is stimulated in part by mitogen- and nutrient-sensing (and other) signaling pathways such as mTOR. Aging, 'an aimless continuation of developmental program', is driven by the same signaling pathways including mTOR. Aging in turn causes damage: not molecular damage but non-random organ damage (stroke, infarction, renal failure and so on) and death. Seemingly, one objection to this concept is that cancer is caused by molecular damage. And cancer is often a cause of death in mammals. So how may one claim that damage does not drive aging, if it is involved in cancer. Let us discuss this."
I have not reviewed the paper yet, but the concept of programmed aging offers an explanation for the acceleration of premature aging witnessed in progeria and werner syndrome where young kids rapidly age into old men and women in just a few years without the assistance of free radical damage, etc. The normal aging paradigm goes into fast forward mode thus by-passing all of the typical wear and tear normally attributed to cellular degeneration. Something I address in my white paper on reversing premature aging by optimizing the expression of our genes. It's the various imbalances in our body chemistry due to environmental factors that sets the stage for our genes to express poorly / out of sync with our biological programming.